NF-κB proteins are transcription factors that integrate inflammatory cytokines, pattern-recognition inputs, and stress signals into gene programs for immune mediators.
What it is
NF-κB typically refers to Rel-family dimers retained in the cytoplasm by IκB proteins until upstream kinase activation triggers nuclear translocation. It is a hub on inflammatory signaling maps.
How it works
Canonical activation proceeds through IKK-mediated IκB phosphorylation, proteasomal IκB degradation, and NF-κB nuclear entry. Target genes include cytokines, chemokines, and survival factors.
Non-canonical branches and extensive feedback mean NF-κB is a network, not a binary on/off switch.
Biological role
The pathway supports host defense and tissue stress responses. Persistent activation themes appear in chronic inflammation literature. Peptide studies that report NF-κB markers should identify cell type and stimulus.
Proteins involved
- IKK complex
- IκBα
- p65/RelA
- p50
- Upstream receptors (TNFR, TLRs, and others)
Research summary
Cell signaling reviews detail activation logic and feedback. Experimental peptide papers often use phospho-p65 or reporter assays as readouts—interpret those as pathway engagement markers, not clinical endpoints.
Descriptions summarize published mechanistic frameworks. Findings from cell culture or animal models should not be interpreted as proven clinical effects in humans.
Research limitations
Scientific references
- Hayden MS, Ghosh S. NF-κB signaling reviews in Genes & Development and related journals.
- Liu T et al. NF-κB in inflammation surveys.